PMID- 9705578
OWN - NLM
STAT- MEDLINE
DCOM- 19980924
LR  - 20181201
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 68
IP  - 2
DP  - 1998 Aug
TI  - Role of corticotropin-releasing hormone in gastrin-releasing peptide-mediated 
      regulation of corticotropin and corticosterone secretion in male rats.
PG  - 116-22
AB  - Gastrin-releasing peptide (GRP) exerts several functions within the hypothalamus 
      and may be involved in the regulation of pituitary hormone secretion. The purpose 
      of this study was to investigate the central effect of GRP on 
      hypothalamic-pituitary-adrenal axis activity in the male rat. 
      Intracerebroventricular (i.c.v.) but not intravenous administration of GRP (1, 
      10, 100 ng/rat) increased plasma ACTH and corticosterone concentrations in a 
      dose-dependent manner. The highest dose (100 ng/rat) of GRP increased plasma ACTH 
      and corticosterone 4- and 14-fold, respectively. This increase peaked at 30-60 
      min after i.c.v. injection, decreased gradually and returned to baseline levels 
      240 min after GRP administration. The i. c.v. administration of 
      (Leu13-psi-CH2NH-Leu14) bombesin, a competitive and specific GRP receptor 
      antagonist, had no effect on ACTH and corticosterone secretion; however, a dose 
      of 1 microg/rat completely blocked the increase of both hormones induced by GRP 
      (10 ng). By using alpha-helical (9-41) corticotropin-releasing factor (CRF), a 
      competitive antagonist of CRF, the role of CRF on GRP-induced ACTH and 
      corticosterone secretion was also explored. alpha-Helical (9-41) CRF (10 
      microg/rat) blocked the increase in ACTH and corticosterone secretion induced by 
      GRP (10 ng). The results obtained in this study suggest that GRP increases the 
      secretion of ACTH and corticosterone in the plasma by acting centrally on GRP 
      receptors, and that endogenous GRP receptor ligands do not tonically regulate 
      ACTH and corticosterone secretion. Furthermore, the 
      hypothalamus-pituitary-adrenal-activating effects induced by GRP appear to be 
      mediated, at least in part, by CRF.
FAU - Garrido, M M
AU  - Garrido MM
AD  - Departamento de Farmacologia, Facultad de Farmacia and Instituto 
      Pluridisciplinar, Universidad Complutense de Madrid, Madrid, Espana.
FAU - Martin, S
AU  - Martin S
FAU - Ambrosio, E
AU  - Ambrosio E
FAU - Fuentes, J A
AU  - Fuentes JA
FAU - Manzanares, J
AU  - Manzanares J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 80043-53-4 (Gastrin-Releasing Peptide)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
RN  - PX9AZU7QPK (Bombesin)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Adrenal Cortex/metabolism
MH  - Adrenocorticotropic Hormone/*metabolism
MH  - Animals
MH  - Bombesin/pharmacology
MH  - Corticosterone/*metabolism
MH  - Corticotropin-Releasing Hormone/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Gastrin-Releasing Peptide/*metabolism
MH  - Hypothalamo-Hypophyseal System/drug effects/metabolism
MH  - Injections, Intraventricular
MH  - Male
MH  - Radioimmunoassay
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 1998/08/15 02:15
MHDA- 2000/08/16 11:00
CRDT- 1998/08/15 02:15
PHST- 1998/08/15 02:15 [pubmed]
PHST- 2000/08/16 11:00 [medline]
PHST- 1998/08/15 02:15 [entrez]
AID - nen68116 [pii]
AID - 10.1159/000054357 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1998 Aug;68(2):116-22. doi: 10.1159/000054357.